All publications mentioned herein are incorporated by reference to the same extent as if each individual publication or patent application was specifically and individually indicated to be incorporated by reference. The following description includes information that can be useful in understanding the present subject matter. It is not an admission that any of the information provided herein is prior art or relevant to the presently claimed subject matter, or that any publication specifically or implicitly referenced is prior art.
Eosinophilic esophagitis (EoE) is a chronic, food antigen-driven, tissue-specific esophageal, inflammatory disease of the esophagus. EoE is characterized by marked mucosal eosinophil accumulation that is often associated with fibrosis, stricture formation, and impaired motility (Liacouras, C. A. et al., J Allergy Clin Immunol 128:3-20 e6, quiz 21-2 (2011); Rothenberg, M. E. Gastroenterology 137:1238-49 (2009); Collins, M. H. et al. Clin Gastroenterol Hepatol 6:621-9 (2008); Putnam, P. E. and Rothenberg, M. E. Curr Gastroenterol Rep 11:220-5 (2009)).
Allergens are thought to drive EoE pathogenesis. This is because the disease remits after removal of specific food types, reoccurs upon food re-introduction, is associated with marked dysregulation of esophageal transcripts rich in elements involved in allergic inflammation (e.g. T helper cell type 2 (Th2) cytokines such as interleukin (IL)-13, eosinophils, and mast cells), and can be induced in mice by allergen exposure through IL-5- and IL-13-driven pathways (Abonia, J. P. and Rothenberg, M. E. Annu Rev Med 63:421-34 (2012); Davis, B. P. and Rothenberg, M. E. Expert Rev Clin Immunol 9:285-7 (2013); Henderson, C. J. et al. J Allergy Clin Immunol 129:1570-8 (2012); Rothenberg, M. E. et al. J Allergy Clin Immunol 130:617-9 (2012)).